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LncRNA FOXD2-AS1 Regulates miR-25-3p/Sema4c Axis To Promote The Invasion And Migration Of Colorectal Cancer Cells
PURPOSE: Although the roles of lncRNA FOXD2-AS1 have been investigated in many types of cancers including colorectal cancer (CRC), its functionality remains to be further investigated. Analysis of the TCGA data set revealed that FOXD2-AS1 was up-regulated in CRC tissues. This study aimed to analyze...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927494/ https://www.ncbi.nlm.nih.gov/pubmed/31908535 http://dx.doi.org/10.2147/CMAR.S228628 |
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author | Zhang, Mengyan Jiang, Xiang Jiang, Sumei Guo, Zhongying Zhou, Qinfeng He, Jingdong |
author_facet | Zhang, Mengyan Jiang, Xiang Jiang, Sumei Guo, Zhongying Zhou, Qinfeng He, Jingdong |
author_sort | Zhang, Mengyan |
collection | PubMed |
description | PURPOSE: Although the roles of lncRNA FOXD2-AS1 have been investigated in many types of cancers including colorectal cancer (CRC), its functionality remains to be further investigated. Analysis of the TCGA data set revealed that FOXD2-AS1 was up-regulated in CRC tissues. This study aimed to analyze the function of FOXD2-AS1 in CRC. METHODS: FOXD2-AS1 expression was detected by qPCR. A 5-year follow-up study was performed to analyze the prognostic value of FOXD2-AS1 for CRC. Overexpression experiments were performed to analyze the interactions among FOXD2-AS1, miR-25-3p and Sema4C. Transwell assays were performed to analyze cell invasion and migration. RESULTS: In this study, we further confirmed the up-regulation of FOXD2-AS1 in CRC patients and showed that high FOXD2-AS1 level predicted poor survival. Bioinformatics analysis showed that miR-25-3p may bind FOXD2-AS1, while over-expression experiments showed no effects on each other’s expression. Instead, FOXD2-AS1 over-expression led to the up-regulate Sema4C, which is a target of miR-25-3p. Transwell assay showed that FOXD2-AS1 and Sema4C over-expression led to the increased invasion and migration rates of CRC cells. MiR-25-3p plays the opposite role and attenuated the effects of FOXD2-AS1 and Sema4C over-expression. CONCLUSION: FOXD2-AS1 may regulate the miR-25-3p/Sema4C axis to promote the invasion and migration of CRC cells. |
format | Online Article Text |
id | pubmed-6927494 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-69274942020-01-06 LncRNA FOXD2-AS1 Regulates miR-25-3p/Sema4c Axis To Promote The Invasion And Migration Of Colorectal Cancer Cells Zhang, Mengyan Jiang, Xiang Jiang, Sumei Guo, Zhongying Zhou, Qinfeng He, Jingdong Cancer Manag Res Original Research PURPOSE: Although the roles of lncRNA FOXD2-AS1 have been investigated in many types of cancers including colorectal cancer (CRC), its functionality remains to be further investigated. Analysis of the TCGA data set revealed that FOXD2-AS1 was up-regulated in CRC tissues. This study aimed to analyze the function of FOXD2-AS1 in CRC. METHODS: FOXD2-AS1 expression was detected by qPCR. A 5-year follow-up study was performed to analyze the prognostic value of FOXD2-AS1 for CRC. Overexpression experiments were performed to analyze the interactions among FOXD2-AS1, miR-25-3p and Sema4C. Transwell assays were performed to analyze cell invasion and migration. RESULTS: In this study, we further confirmed the up-regulation of FOXD2-AS1 in CRC patients and showed that high FOXD2-AS1 level predicted poor survival. Bioinformatics analysis showed that miR-25-3p may bind FOXD2-AS1, while over-expression experiments showed no effects on each other’s expression. Instead, FOXD2-AS1 over-expression led to the up-regulate Sema4C, which is a target of miR-25-3p. Transwell assay showed that FOXD2-AS1 and Sema4C over-expression led to the increased invasion and migration rates of CRC cells. MiR-25-3p plays the opposite role and attenuated the effects of FOXD2-AS1 and Sema4C over-expression. CONCLUSION: FOXD2-AS1 may regulate the miR-25-3p/Sema4C axis to promote the invasion and migration of CRC cells. Dove 2019-12-19 /pmc/articles/PMC6927494/ /pubmed/31908535 http://dx.doi.org/10.2147/CMAR.S228628 Text en © 2019 Zhang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Zhang, Mengyan Jiang, Xiang Jiang, Sumei Guo, Zhongying Zhou, Qinfeng He, Jingdong LncRNA FOXD2-AS1 Regulates miR-25-3p/Sema4c Axis To Promote The Invasion And Migration Of Colorectal Cancer Cells |
title | LncRNA FOXD2-AS1 Regulates miR-25-3p/Sema4c Axis To Promote The Invasion And Migration Of Colorectal Cancer Cells |
title_full | LncRNA FOXD2-AS1 Regulates miR-25-3p/Sema4c Axis To Promote The Invasion And Migration Of Colorectal Cancer Cells |
title_fullStr | LncRNA FOXD2-AS1 Regulates miR-25-3p/Sema4c Axis To Promote The Invasion And Migration Of Colorectal Cancer Cells |
title_full_unstemmed | LncRNA FOXD2-AS1 Regulates miR-25-3p/Sema4c Axis To Promote The Invasion And Migration Of Colorectal Cancer Cells |
title_short | LncRNA FOXD2-AS1 Regulates miR-25-3p/Sema4c Axis To Promote The Invasion And Migration Of Colorectal Cancer Cells |
title_sort | lncrna foxd2-as1 regulates mir-25-3p/sema4c axis to promote the invasion and migration of colorectal cancer cells |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927494/ https://www.ncbi.nlm.nih.gov/pubmed/31908535 http://dx.doi.org/10.2147/CMAR.S228628 |
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